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PubMed1979

Tumor-specific immunity induced by somatic hybrids. II. Elicitation of enhanced immunity against the parent plasmacytoma.

Hybrid cells derived from fusion of a BALB/c plasmacytoma (TEPC-15) and L cells (C3H origin) were used to stimulate tumor-specific immunity against the parental plasmacytoma cells. Live hybrid cells induced tumor-specific immunity against TEPC-15 more effectively than mitomycin-treated hybrid or TEPC-15 tumor cells. Adoptive transfer of immunity with spleen cells of mice immunized with hybrid cells was also more effective than that with mitomycin-treated tumor cells. The immunity induced by the hybrid cells was specific to the TEPC-15 tumor because the mice that received immune spleen cells were not protected against challenge with either HOPC-8 or McPC-603 plasmacytomas. T cell populations were primarily responsible for the transfer of specific immunity based on the sensitivity of immune cells to anti-Thy 1.2 and complement. Mice that had established solid tumors were treated with 5 x 10(7) spleen cells to evaluate the therapeutic value of the hybrid-induced immune cells. Tumors in the mice that received immune cells gradually regressed over a 40-day period, whereas tumors on the control mice continued to grow. These results suggest that a rearrangement of tumor-specific antigens on allogeneic hybrid cells can enhance their immunogenicity.

Animals↗

PubMed1976

Adoptive transfer of immunity to Plasmodium berghei with immune T and B lymphocytes.

Immunity to malarial infection may be transferred with immune lymphocytes. This study was designed to determine which lymphocyte type is responsible for the adoptive transfer of immunity to malarial infection. In one set of experiments, the ability of immune T and B lymphocytes, separated by passage through nylon-wool columns, to transfer immunity to infection was determined. In another experiment, the effect of killing T lymphocytes with anti-theta serum on the transfer of immunity was determined. The effect on the ability of immune lymphocyte suspensions to transfer immunity after B lymphocytes were removed from such suspensions by centrifugation on Ficoll-Hypaque gradients, after they had formed rosettes with sensitized, complement-coated sheep erythrocytes, was also determined. The ability of lymphocyte suspensions to adoptively transfer resistance to malarial infection was greatly impaired by the removal from the suspensions of differentiated B-type lymphocytes. Our results indicate that it is the differentiated B cell, most probably an antibody-producing cell, which lacks both theta antigen and the complement receptor that is responsible for conferring immunity to malaria.

Animals↗

PubMed1991

Immunization with subunit human immunodeficiency virus vaccine generates stronger T helper cell immunity than natural infection.

Healthy, human immunodeficiency virus seronegative (HIV-) volunteers were multiply immunized with a recombinant gp160 (rgp160) candidate acquired immunodeficiency syndrome (AIDS) vaccine. Peripheral blood lymphocytes from volunteers immunized with 40 micrograms or with 80 micrograms (two volunteers per group) of rgp160, as well as from control donors, were tested for T helper (Th) cell function either prior to immunization, 8 to 12 months after the third immunization, or 2 to 5 months after the fourth immunization. The Th cell functional tests included antigen-induced in vitro interleukin 2 (IL 2) production and proliferation in response to influenza A virus (FLU) and to four synthetic peptides of HIV gp120 and gp160, previously demonstrated to be recognized by T cells from HIV naturally infected patients. Our results demonstrate the following: (a) immunization of HIV- individuals with rgp160 results in IL 2 production and T cell proliferation in response to HIV determinants; (b) boosting with rgp160 enhances Th function; (c) HIV-specific Th function is up to 100-fold greater in the multiply immunized volunteers than that observed in asymptomatic, HIV-infected individuals; and (d) multiple immunization with rgp160 does not impair Th function to a non-HIV antigen such as influenza A virus. These results indicate that immunization of uninfected individuals with an HIV subunit vaccine results in much stronger Th cell immunity than does natural infection and suggests that vaccination against HIV may be possible.

Gene Products, env↗

PubMed1995

Systemic immunization induces protective CD4+ and CD8+ T cell-mediated immune responses in murine Listeria monocytogenes meningoencephalitis.

The immune mechanisms underlying immunization-induced protection of mice from lethal central nervous system (CNS) listeriosis were evaluated by immunohistochemistry, flow cytometry of leukocytes isolated from the brain, reverse transcription-polymerase chain reaction analysis of intracerebral (i.c.) tumor-necrosis factor-alpha, interferon-gamma, interleukin (IL)-2, IL-1 beta, IL-10, granulocyte/macrophage colony-stimulating factor, and inducible nitric oxide synthase mRNA expression, and T cell depletion experiments. The data demonstrate that active immunization of mice prior to an i.c. infection with Listeria monocytogenes prevents the development of a fatal necrotizing encephalitis and accelerates the recruitment of an increased number of alpha beta T cell receptor (TcR)+ CD4+ and CD8+ T cells, gamma delta TcR+ T cells, B cells, granulocytes and macrophages to the brain compared to non-immunized animals. In addition, immunization induced a pronounced activation of i.c. macrophages and microglial cells as shown by an increased expression of MHC class II antigens. In parallel, transcript levels for all cytokine mRNA analyzed were higher in the brains of immunized mice. The protective effects of immunization were completely abolished by depletion of CD4+, CD8+, or both T cell subsets. All groups of T cell-depleted immunized mice developed a fatal necrotizing encephalitis with an increased i.c. bacterial load. In addition, cytokine mRNA synthesis was significantly impaired. The severity of disease was only slightly different between CD4+, CD8+ and CD4+/CD8+ T cell depleted mice, indicating that both subsets of T cells are required for an effective i.c. immune response to L. monocytogenes. This is in marked contrast to systemic listeriosis, and points to CNS-specific features of the immune response.

Animals↗

PubMed2001

Induction of antigen-specific Th1-biased immune responses by plasmid DNA in schistosoma-infected mice with a preexistent dominant Th2 immune profile.

A requisite for vaccines to confer protection against intracellular infections such as Human Immunodeficiency Virus or Mycobacterium tuberculosis is their capacity to induce Th1 immune responses. However, they may fail to do so in Africa and South East Asia, where most individuals have a dominant preexistent Th2 immune profile, due to persistent helminthic parasitic infections, which may undermine any Th1 response. It is well established that DNA vaccines induce strong Th1 biased immune responses against an encoded antigen, depending on the route and mode of immunization. Here, we demonstrate that intradermal immunization with plasmid DNA encoding beta-gal (pCMV-LacZ) of Schistosoma-infected mice, with preexistent dominant Th2 immune background, induce a strong Th1 anti-beta-gal response, as opposed to immunized with beta-gal only. Importantly, the established protective Th2 immune response to schistosomes was not disrupted. These findings strongly support the possibility of using plasmid DNA as a Th1 inducing adjuvant when immunizing populations with a strong preexistent Th2 immune profile.

Animals↗

PubMed1993

Induction of immune-mediated glomerulonephritis in normal mice immunized with bacterial DNA.

Normal mice immunized with bacterial DNA produce high titers of anti-DNA antibodies and represent a new model for autoantibody production in systemic lupus erythematosus. To determine whether DNA immunization can also provoke clinical manifestations of lupus, the occurrence of nephritis in immunized mice was assessed and correlated with levels of anti-DNA as well as antibodies to glomerular antigens. BALB/c mice immunized with Escherichia coli single-stranded DNA in complexes with methylated bovine serum albumin in adjuvant showed increased proteinuria compared to control mice immunized with mBSA alone. Furthermore, DNA immunized mice had significantly greater glomerular proliferative changes and immunoglobulin deposition than control mice. In an in vitro assay, sera from DNA immunized mice exhibited greater binding to glomerular antigens than sera from control mice. Compared to sera, renal eluates from DNA-immunized mice were enriched for anti-DNA and glomerular binding activity. These data indicate that immunization of normal mice with E. coli DNA induces an immune-mediated proliferative glomerulonephritis that is likely secondary to the renal deposition of anti-DNA antibodies.

Animals↗

PubMed1986

Cells involved in the immune response. XXXI. The role of the spleen in the primary and secondary immune responses in the normal adult outbred rabbit: the initial localization of memory cells to the spleen and their subsequent dissemination to the thymus and peripheral lymph nodes.

Normal adult outbred rabbits were immunized intravenously (iv) with sheep erythrocytes (SRBC). At varying times thereafter, the different lymphoid organs were investigated for spontaneous and culture-induced antibody secreting cells by the aqueous hemolytic plaque-forming cell (PFC) technique. During the phase of active antibody formation (Days 3 to 30), immediate PFC, indicative of spontaneous antibody synthesis and secretion, were detected principally in the spleen. In the early postimmune memory period (Days 30 to 90), memory cells capable of generating PFC following secondary immunization in in vitro culture with SRBC were detected only in the spleen. However, by 4 months postimmunization, memory cells were detected in the thymus and popliteal lymph node (PLN) as well as in the spleen. The number of memory cells in the thymus and PLN was significantly higher by 6 months postprimary iv immunization and was even further elevated by 9 months postprimary iv immunization. Following in vivo secondary immunization by the iv injection of SRBC 2 or 6 months postprimary immunization, immediate PFC were detected in large numbers in the spleen, the bone marrow, and the blood, marginally in the PLN and not at all in the thymus. Similar results were obtained at 9 months following primary immunization with SRBC with the exception that large numbers of immediate PFC were detected in the PLN following secondary iv immunization. Following culture of these lymphoid cells for 5 days in vitro with SRBC, the thymus and PLN cells, as well as the spleen cells, generated large numbers of PFC. Since immediate PFC were never detected among the freshly isolated thymus cells whereas thymic cell cultures 6 and 9 months postprimary iv immunization invariably generated large numbers of PFC following secondary immunization in vitro, the thymus memory cells would appear to be inaccessible to particulate antigen injected intravenously; they can only be detected following activation by the antigen in culture. The PFC generated by thymus memory cells (and spleen and PLN) were totally inhibited by the inclusion of sheep anti-rabbit IgG into the PFC assay. This finding demonstrates unequivocally that the plaques induced by thymus cells, just as the plaques induced by spleen and PLN cells, are antibody mediated and not false plaques. Therefore, the thymic PFC cells must be antibody-secreting B-memory cells since T cells do not synthesize or secrete immunoglobulins.

Animals↗

PubMed2004

Mucosal immunization with purified flagellin from Salmonella induces systemic and mucosal immune responses in C3H/HeJ mice.

This study investigated the immune response elicited in C3H/HeJ mice after oral, parenteral and nasal immunization with purified flagellin from Salmonella enterica serovar Enteritidis alone or conjugated to starch microparticles as adjuvant or together with the uptake-enhancer recombinant cholera toxin B-subunit (rCTB). Systemic (IgM-IgG, IgA, IgG2a, IgG2b, IgG1) and local (s-IgA) humoral immune responses in the mice were analyzed using enzyme-linked immunosorbent assays (ELISA). Primed splenocytes were also stimulated in vitro with flagellin and the supernatants analyzed for cytokine production. Finally, immunized mice were challenged orally with live Salmonella. A high flagellin-specific IgM-IgG response was seen in all groups, especially in mice immunized nasally with flagellin plus rCTB or subcutaneously, but a strong systemic antibody response was also induced when free antigen was given orally. Intranasal or subcutaneous immunization of mice with flagellin plus rCTB or oral immunization with flagellin plus microparticles resulted in a significantly greater mucosal response (higher s-IgA titers in feces) than seen in the control group (P <0.05). The mucosal IgA responses were significantly correlated with the serum IgA titers. The subclass profile in serum revealed a mixed Th1/Th2-type response, with a predominance of Th1-type, as indicated by the subclass ratio (IgG1/IgG2a + IgG2b). The splenocytes stimulated in vitro produced interferon (IFN)-gamma, at levels, which increased with time. The group immunized with flagellin plus rCTB subcutaneously had a relatively higher IFN-gamma response than the other groups. Interleukin (IL)-2 was also produced, especially in mice immunized nasally or subcutaneously with flagellin conjugated to microparticles. However, neither IL-4 nor IL-5 was produced in any of the groups. After oral challenge with live serovar Enteritidis, the groups immunized orally or nasally with free flagellin had significantly lower degree of infection than the control group (P <0.05).

Adjuvants, Immunologic↗

PubMed2005

Enhanced mucosal and systemic immune response with intranasal immunization of mice with HIV peptides entrapped in PLG microparticles in combination with Ulex Europaeus-I lectin as M cell target.

The predominant route of HIV infection is through the sexual transmission via M cells. Most of the peptide and protein vaccines show poor transport across the epithelial barrier and are commonly administered by parenteral route. In the present study four HIV peptides from envelope (gp 41-LZ (leucine zipper), gp 41-FD (fusion domain) and gp120-C2) and regulatory (Nef) region in poly lactic-co-glycolide (PLG) micro-particle delivery were evaluated in mice of outbred and with different genetic background to compare immune response versus MHC restriction. Out of the combinational and single routes of immunization attempted, the single route maintained the IgG, IgA and sIgA in sera and washes for longer duration as compared to combinational routes in which the response was declined. The study demonstrated that single intranasal immunization offered significantly higher immune response (p<0.05) over oral and rectal mucosal routes in terms of inducing systemic as well as mucosal response. Also, the specific activity measurement of IgA and IgG in sera and sIgA in washes were correlating to the antibody titers. However, the intramuscular route of immunization generated systemic response only. The entrapment of plant lectin UEA-1 a ligand specific for M cells in micro-particle further enhanced the immune response in all the mucosal routes. The IgG isotypes generated were of IgG1 and IgG2a/2b in sera for all the peptides. The T cell proliferation response study with and without UEA-1 lectin in micro-particles showed significantly high (p<0.05) stimulation index (SI) with intranasal immunization for all the peptides from cells collected from spleen (SP), peyer's patches (PP) and lamina propria (LP) with SI in the order LP cells>PP>or=SP. The cytokine measurement profile of IL-2, IFN-gamma and IL-6 and low levels of IL-4 in the cultural supernatants of SP, PP and LP showed mixed CD4(+) Th1 and Th2 immune response. The p24 assay showed high percent inhibition of HIV-IIIB virus with sera and washes obtained from intranasal route. Thus, overall the study highlighted the combination of UEA-1 lectin with HIV peptides in micro-particles through intranasal immunization generated systemic as well as mucosal immune response.

AIDS Vaccines↗

PubMed2001

Fusion of C3d molecule with bovine rotavirus VP7 or bovine herpesvirus type 1 glycoprotein D inhibits immune responses following DNA immunization.

The binding of the complement C3d molecule with receptors on B cells and/or follicular dendritic cells (FDCs) influences the induction of humoral immune responses. For example, C3d fused to an antigen has been shown to have a strong adjuvant effect on antibody production. We investigated the possibility that co-expression of antigen and C3d as a fusion protein could enhance antigen-specific immune responses, following plasmid immunization. One or two copies of murine C3d-cDNA, C3d or (C3d)(2), respectively, were cloned together with bovine rotavirus (BRV) VP7 or bovine herpesvirus type 1 (BHV-1) glycoprotein D (gD) genes. All constructs contained a signal peptide that resulted in the secretion of the expressed proteins. In vitro, the characterization of the chimeric proteins indicated that both VP7 and gD retained their antigenicity and the C3d remained biologically active. However, immunization with plasmids encoding VP7-C3d chimeras did not enhance rotavirus-specific antibody responses and the frequency of BRV-specific IFN-gamma secreting cells in the spleens were significantly lower in mice immunized with pVP7-(C3d)(2) when compared with mice immunized with plasmid encoding VP7. The same pattern of immune responses was observed for plasmids encoding gD-C3d. Both gD-specific antibody responses and the frequency of gD-specific IFN-gamma secreting cells were significantly lower in mice immunized with plasmid expressing gD-C3d chimeras when compared with mice immunized with plasmid encoding gD alone. These results indicate that co-expression of C3d with an antigen actually inhibit both humoral and cell-mediated antigen-specific immune responses.

Animals↗

PubMed2002

Intranasal immunization with SIV virus-like particles (VLPs) elicits systemic and mucosal immunity.

By using a baculovirus expression system, we have successfully produced simian immunodeficiency virus (SIV)-like particles (VLPs) with high levels of biologically active SIV envelope (Env) incorporated on their surfaces. To study whether SIV VLPs represent effective mucosal immunogens, we immunized groups of mice with VLPs alone or VLPs plus the mucosal adjuvant cholera toxin (CT) by the intranasal (i.n.) route. High levels of serum IgG antibody production were achieved in mice immunized intranasally with SIV VLPs, and the antibody response was found to be antigen dose-dependent. The IgG1 and IgG2a ratio indicates that immune responses induced by SIV VLPs are Th1 oriented. Mice immunized with VLPs plus CT were found to exhibit higher serum antibody responses than those immunized with VLPs alone (P<0.001). Furthermore, IgA antibody production was detected in both saliva and vaginal fluid from mice mucosally immunized with SIV VLPs. Higher levels of IgA were found in vaginal fluid than in saliva in animals immunized with SIV VLPs plus CT (P<0.05). Higher neutralizing activity to SIV 1A11 was also found in serum of animals immunized with SIV VLPs plus CT. Moreover, increased numbers of MHC I-restricted peptide-specific IFN-gamma and IL-4 producing T cells were detected in both splenocytes and lymph nodes by intranasal immunization of SIV VLP plus CT. These results suggest that VLPs are effective mucosal antigens that can induce both humoral and cellular immune responses at systemic and mucosal sites.

Administration, Intranasal↗

PubMed1997

Protection, humoral and cell-mediated immune responses in calves immunized with multiple emulsion haemorrhagic septicaemia vaccine.

A multiple emulsion (ME), vaccine against Pasteurella multocida (P52) infection in cattle was prepared and the efficiency in terms of immunity to direct challenge, duration of this immunity for up to 1 year and the role of humoral and cell-mediated immune mechanisms were studied. ME vaccine was sterile, safe and was potent when tested in rabbits and calves. Nineteen calves were immunized with a single 4 ml dose of ME vaccine intramuscularly. Group of these calves were challenge infected with virulent P. multocida (P52) (10(-1) 18 h old broth culture) given by the subcutaneous route at 21 days, 3 months, 6 months, 9 months and 1 year. All the immunized calves withstood challenge infection and showed 100% protection. Humoral immune response was measured by indirect haemagglutination test (IHA) and enzyme-linked immunosorbant assay (ELISA). Statistically ELISA values were found to be superior to IHA values because of small coefficient of variance. A fall in mean antibody titres during 24 h, 48 h, post-challenge infection was recorded whereas a steady increase in the titre after 72 h up to 10 days was noticed. The prechallenge mean titre in animals correlated with survival of animals. Humoral antibodies were detected as early as 7 day post-immunization and persisted to 1 year after immunization. Leucocyte migration inhibition test showed > 20% migration inhibition during all pre- and post-challenge periods in animals suggesting an involvement of cell-mediated immune mechanism in protection. Our findings suggested that both humoral and cell-mediated immune responses contribute to protection in vaccinated animals. The results of these studies of ME vaccine showed that it can be successfully used for the effective control of haemorrhagic septicaemia.

Animals↗

PubMed1997

DNA immunization can stimulate florid local inflammation, and the antiviral immunity induced varies depending on injection site.

DNA immunization is being considered to augment, or even to supplant, more traditional methods of antiviral immunization. Different routes of administration lead to markedly different levels of marker protein expression, but only limited data are available concerning the antiviral responses induced by DNA inoculated by different routes, and their protective efficacy. In this report we evaluate antiviral immunity induced by inoculation of DNA by the intramuscular (i.m.) and intradermal (i.d.) routes, and make three novel observations. First, i.d. immunization is dose-dependent and, although not uniformly successful, can induce very high levels of cytotoxic T lymphocyte (CTL) activity, varying dependent on the vehicle in which the DNA is administered. Second, while antiviral immunity induced by i.m. DNA injection has been demonstrated by many groups, we show herein a marked difference in immunity depending on the muscle injected. Immunity induced by DNA injection of the anterior tibial muscle significantly exceeds that induced following injection of the quadriceps muscle as judged by three criteria, namely CTL induction, decrease in virus titer following nonlethal challenge, and survival following a normally lethal challenge dose of virus. Thirdly, we evaluate the local immune response induced following immunization with DNA encoding a viral antigen. We show that, when recipients are already immune to the encoded protein, a severe but localized inflammatory response may result.

Animals↗

PubMed2003

Immunity to melanoma: unraveling the relation of tumor immunity and autoimmunity.

Cancer cells express self-antigens that are weakly recognized by the immune system. Even though responses against autologous cells are difficult to induce, the immune system is still able to mount a response against cancer. The discovery of the molecular identity of antigens that are recognized by the immune system of melanoma patients has led to the elucidation of tumor immunity at a cellular and molecular level. Multiple pathways in both the priming and effector phases of melanoma rejection have been described. Animal models' active immunotherapies for melanoma show a requirement for the cellular compartment of the immune system in the priming phase, primarily CD4+T cells. More diverse elements are required for the effector phase, including components from the innate immune system (macrophages, complement and/or natural killer cells) and from the adaptive immune system (CD8+T cells and B cells). Minor differences in amino-acid sequences of antigens must determine the particular mechanisms involved in tumor rejection. Since the immune system contains T and B cells that recognize and reject autologous cells, a consequence of tumor immunity is potential autoimmunity. There are distinct pathways for tumor immunity and autoimmunity. The requirements for autoimmunity at the priming phase seem to be CD4+/IFN-gamma dependent while the effector mechanisms are alternative and redundant. Vitiligo (autoimmune hypopigmentation) can be mediated by T cells, FcgammaR+macrophages and/or complement.

Animals↗

PubMed2003

The war between the malaria parasite and the immune system: immunity, immunoregulation and immunopathology.

Throughout history malaria has proved to be a significant threat to human health. Between 300 and 500 million clinical cases occur each year worldwide, approximately 2 million of which are fatal, primarily in children. The vast majority of malaria-related deaths are due to infection with Plasmodium falciparum; P. vivax causes severe febrile illness but is rarely fatal. Following repeated exposure to infection, people living in malaria endemic areas gradually acquire mechanisms to limit the inflammatory response to the parasite that causes the acute febrile symptoms (clinical immunity) as well as mechanisms to kill parasites or inhibit parasite replication (antiparasite immunity). Children, who have yet to develop protective immune mechanisms are thus at greater risk of clinical malaria, severe disease and death than adults. However, two epidemiological observations indicate that this is, perhaps, an oversimplified model. Firstly, cerebral malaria - a common manifestation of severe malaria - typically occurs in children who have already acquired a significant degree of antimalarial immunity, as evidenced by lower mean parasite densities and resistance to severe anaemia. One potential explanation is that cerebral malaria is, in part, an immune-mediated disease in which immunological priming occurs during first infection, eventually leading to immunopathology on re-infection. Secondly, among travelers from nonendemic areas, severe malaria is more common - and death rates are higher - in adults than in children. If severe malaria is an immune-mediated disease, what might be priming the immune system of adults from nonendemic areas to cause immunopathology during their first malaria infection, and how do adults from endemic areas avoid severe immunopathology? In this review we consider the role of innate and adaptive immune responses in terms of (i) protection from clinical malaria (ii) their potential role in immunopathology and (iii) the subsequent development of clinical immunity. We conclude by proposing a model of antimalarial immunity which integrates both the immunological and epidemiological data collected to date.

Adult↗

PubMed1998

Measles immunity and immunization status in under-5-year-old children in New South Wales: a population-based study.

OBJECTIVE: To estimate the proportion of 1-4-year-old New South Wales children immune to measles and compare the documented immunization history with serologically defined immune status. DESIGN: Population based seroprevalence survey piggybacked onto the National Survey of Lead in Children. Immune status was determined by two different enzyme immunoassays on plasma samples from subjects. SETTING: New South Wales, February-March 1995. OUTCOME MEASURES: Documented measles immunization collected by interview survey and serologically defined immunity. RESULTS: Of 689 survey subjects, 430 (62.4%) provided a blood sample. Adequate plasma remained for both assays for 347 children, of whom 279 (80.4%) were immune by both assays. Parents of 330 stated that their children were immunised, of whom 211 (63.9%) were able to produce corroborating records. Of these 211 subjects, 178 (84.4%) were immune compared to 87 (76.3%) of 114 without records (P = 0.07). CONCLUSIONS: We estimate the prevalence of true measles immunity in 1-4-year-old NSW children to be only 80%, a level inadequate to prevent outbreaks of measles in urban populations. Both long term and immediate strategies are required to increase the prevalence of immunity among NSW children; these may include lowering the age of the routine second measles dose and mounting a mass measles immunisation campaign to include preschool aged children.

Chi-Square Distribution↗

PubMed1998

Induction of immunity in the respiratory tract and protection from bovine herpesvirus type 1 infection by different routes of immunization with recombinant adenovirus.

To investigate the capability of different routes of immunization with replication-competent recombinant adenovirus to induce antigen-specific antibody responses, we immunized cotton rats with a human adenovirus type 5 (HAd5) vector expressing the glycoprotein D (gD) of bovine herpesvirus type 1 (BHV-1) (gD-dE3). Different routes of mucosal and systemic immunization (intraduodenal-oral, intraduodenal, intranasal and intradermal) with gD-dE3 stimulated similar levels of gD-specific IgG in the serum of cotton rats. However, intranasal (i.n.) immunization stimulated higher levels of gD-specific IgA in the lung and nasal washes, and higher frequency of gD-specific antibody secreting cells in the lung than did the intradermal immunization. Higher levels of antibody in the respiratory tract following i.n. immunization correlated with better protection of the lungs against i.n. BHV-1 challenge. Intraduodenal-oral immunization induced more gD-specific antibodies in the respiratory tract than intraduodenal immunization alone. Adenovirus dissemination to most organs tested was evident following each route of immunization, which is important to consider when studying the mechanism of induction of immunity by recombinant adenoviruses.

Adenoviruses, Human↗

PubMed1979

Assessment of host immune status during progressive growth and after excision of DNA virus (simian virus 40) tumors in hamsters: comparison of tumor-specific and tumor-unrelated parameters of immune responsiveness.

The kinetics of cell-mediated immunity to simian virus 40 (SV40) tumor-specific transplantation antigen (TSTA) were compared to the kinetics of tumor-unrelated parameters of immune responsiveness in the assessment of the immune statuses of inbred MHA/SsLAK hamsters during the course of progressive syngeneic SV40 tumor growth and after tumor excision. With the use of the tumor cell neutralization test in vivo and the macrophage migration inhibition assay in vitro, specific cellular immunity to SV40 TSTA was detected by 4 days after tumor cell inoculation, when the tumor was small. This tumor-specific immune response was no longer detected at 7 days after tumor cell inoculation, when the tumor had reached a mean diameter of 12.5 mm, but it returned by 14 days after surgical excision of the tumor. The patterns of host responsiveness to mitogens in spleen cells derived from tumor-bearing animals or from tumor-excised animals generally showed little or no correlation with the kinetics of tumor-specific cellular immunity. The kinetics of the humoral immune response to murine erythrocytes, as determined by hemagglutination assays, correlated much more closely with the kinetics of tumor-specific immunity than did the responses to mitogens. IgG antibody (T-dependent) responses were more affected by progressive tumor growth than were IgM antibody (T-independent) responses. The data suggest that results of tests with the use of tumor-unrelated parameters of immune responsiveness for the assessment of the immune status of cancer patients should be interpreted with caution.

Animals↗